IMMUNOTOXICITY OF INVITRO VANADIUM EXPOSURES - EFFECTS ON INTERLEUKIN-1, TUMOR-NECROSIS-FACTOR-ALPHA, AND PROSTAGLANDIN-E2 PRODUCTION BY WEHI-3 MACROPHAGES
Md. Cohen et al., IMMUNOTOXICITY OF INVITRO VANADIUM EXPOSURES - EFFECTS ON INTERLEUKIN-1, TUMOR-NECROSIS-FACTOR-ALPHA, AND PROSTAGLANDIN-E2 PRODUCTION BY WEHI-3 MACROPHAGES, International journal of immunopharmacology, 15(3), 1993, pp. 437-446
Treatment of cultured mouse macrophages with either of two different v
anadium compounds was shown to affect the production/release of two ma
jor immunoregulatory cytokines. The pentavalent vanadium compound ammo
nium metavanadate was shown previously to disrupt cell-mediated immuni
ty at the earliest stages of an in vivo anti-Listerial response, in th
at mice treated with vanadium displayed decreased accessory cell recru
itment and numbers of activated macrophages at infection sites. To det
ermine whether these effects were due to vanadium-induced alterations
in the production of biologically-active mediators, mouse macrophage-l
ike WEHI-3 cells were treated in vitro with ammonium metavanadate or v
anadium pentoxide prior to stimulation with lipopolysaccharide endotox
in (LPS). After stimulation, monokine (tumor necrosis factor-alpha and
interleukin-1) and prostaglandin E2 (PGE2) activities were assessed.
Both vanadium compounds decreased recovered monokine activities; measu
red TNFalpha concentrations were also reduced. Spontaneous release of
the IL-1/TNF-regulating prostanoid PGE2 was significantly increased by
the highest concentration of vanadate tested, although LPS-stimulated
PGE2 production was unaffected by either compound. These results indi
cate that, in vitro, pentavalent vanadium can interfere with immunoreg
ulatory mediators critical for maintaining host immunocompetence.